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戈尔吉蛋白73促进肝细胞癌中的血管生成

Yiming Liu^1,2,3, Xinyang Hu^2,3, Sining Zhou⁴

¹Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province, Hangzhou City University School of Medicine, Hangzhou 310015, China.

Research (Washington, D.C.)

|July 18, 2024

概括

戈尔吉蛋白73 (GP73) 通过稳定缺氧诱导因子-1α (HIF-1α) 和激活Ras-MAPK信号,促进肝细胞癌 (HCC) 血管生成. 向GP73可能为HCC提供一种新的抗血管性疗法.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

戈尔吉蛋白73 (GP73) 在肝细胞癌 (HCC) 中升高,并影响瘤微环境 (TME).
确切地说,GP73影响HCC TME的精确分子机制仍然不完全阐明.

研究的目的:

调查GP73在调节HCC瘤微环境中的血管生成中的作用.
为了确定受GP73在HCC中影响的分子相互作用和信号通路.

主要方法:

研究了GP73与prolyl氧酶-2 (PHD-2) 的相互作用及其对HCC细胞中缺氧诱导的因子-1α (HIF-1α) 氧化的影响.
分析了由人类静脉内皮细胞 (HUVECs) 内部化的外体GP73.
研究了GP73与HECTD1的相互作用及其对生长因子受体结合蛋白2 (GRB2) 稳定性及其对Ras-mitogen-activated protein kinase (MAPK) 途径激活的影响.

主要成果:

GP73具有竞争性抑制PHD-2,减少HIF-1α氧化和增加血管内皮生长因子A (VEGFA) 在HCC细胞中的产生.
来自HCC细胞的外体GP73被HUVEC内部化,在那里它与HECTD1相互作用,稳定GRB2并激活Ras-MAPK通路.
升高的GP73增强了VEGFA的产生,并强化了内皮细胞中的线粒生成信号,促进了TME血管生成.

结论:

通过调节HIF-1α稳定性和激活内皮细胞信号传递,GP73在促进HCC血管生成方面发挥着至关重要的作用.
在HCC血管生成中GP73的功能突出显示了其作为抗血管性策略的治疗点的潜力.

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